Diabetes

Alicia Purdom

Class: English 101

Professor: Mrs. Kravitz-Sheppard

Date: February 5,2004

Diabetes (diabetes mellitus)

Diabetes is a disease characterized by excessive urination. Diabetes mellitus is caused by insufficient insulin production or lack of responsiveness to insulin, resulting in hyperglycemia (high blood glucose levels). There are 2 primary types of diabetes mellitus, type I (insulin-dependent or juvenile-onset), which may be caused by an autoimmune response, and type II (non-insulin-dependent or adult-onset). Diabetes insipidus is typically due to hormonal dysregulation.

Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced in the pancreas by the beta cells of the islets of Langerhans. Absence, destruction, or loss of these cells causes an absolute deficiency of insulin, leading to type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). Most children with diabetes have IDDM and a lifetime dependence on exogenous insulin.

Type 2 diabetes (nonÐ'-insulin-dependent diabetes mellitus [NIDDM]) is a heterogeneous disorder. Patients with NIDDM have insulin resistance, and their beta cells lack the ability to overcome this resistance. Although this form of diabetes previously was uncommon in children, 20% or more of new patients with diabetes in childhood and adolescence now have NIDDM, a change associated with increased rates of obesity.

Insulin is essential to process carbohydrate, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and fat cells and by stimulating the conversion of glucose to glycogen as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. Additionally, insulin slows the breakdown of protein for glucose production.

Hyperglycemia results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with IDDM wastes away and eventually dies from diabetic ketoacidosis.

Information on mortality rates is difficult to ascertain without complete national registers of childhood diabetes, although age-specific mortality probably is double that of the general population. Particularly at risk are children aged 1-4 years who may die with DKA at the time of diagnosis. Adolescents also are a high-risk group. Most deaths result from delayed diagnosis or neglected treatment and subsequent cerebral edema during treatment for DKA, although untreated hypoglycemia also causes some deaths.

IDDM complications are comprised of 3 major categories: acute complications, long-term complications, and complications caused by associated autoimmune diseases. Acute complications reflect the difficulties of